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Novartis AG plans to ramp up its research in Alzheimer’s disease, a potential $20 billion market lacking a major contender and littered with three high-profile drug failures in the past year alone.

“This remains high on our radar, with high unmet medical need,” Tim Wright, who heads the Basel, Switzerland-based company’s drug development, said on a conference call arranged by Sanford C. Bernstein & Co. analyst Tim Anderson in April. Novartis didn’t respond to a request for comment on its Alzheimer’s research.

Novartis would be racing to catch up with Roche Holding AG (ROG) and Merck & Co. (MRK), which are conducting human tests on treatments for Alzheimer’s, the most common dementia illness. Drugmakers are vying to find a way to slow the disease, which may affect 65 million people by 2030. The field is marked with failures, including a study Baxter International Inc. (BAX) released this month in which its Gammagard drug didn’t help patients.

“Should Novartis move into Alzheimer’s? Yes,” Michael Leuchten, an analyst at Barclays Plc in London, said by phone. “Will it be easy to do? No.”

Novartis is pursuing alternatives including licensing agreements, Wright said on the call. So far the drugmaker’s development in the area hasn’t progressed as quickly as Novartis hoped over past years, he said.

Current Drugs

Novartis sells Exelon, a drug that lessens symptoms of the disease by preventing the breakdown of a substance linked to learning and memory. The drug, also used in Parkinson’s disease, may have about $930 million in sales this year, according to analysts’ estimates compiled by Bloomberg. Novartis bought a license to an Alzheimer’s vaccine from Cytos Biotechnology AG in 2003, and the companies completed a mid-stage trial in December.

“Alzheimer’s would really make a lot of sense for Novartis,” Olav Zilian, an analyst at Helvea SA in Geneva, sai

Metal elements and molecules interact in the body but visualizing them together has always been a challenge. Researchers from the RIKEN Center for Life Science Technologies have developed a new molecular imaging technology that enables them to visualize bio-metals and bio-molecules simultaneously in a live mouse. This new technology will enable researchers to study the complex interactions between metal elements and molecules Metal elements and molecules interact in the body but visualizing them together has always been a challenge. Researchers from the RIKEN Center for Life Science Technologies have developed a new molecular imaging technology that enables them to visualize bio-metals and bio-molecules simultaneously in a live mouse. This new technology will enable researchers to study the complex interactions between metal elements and molecules in living organisms.
Metal elements such as zinc, iron and copper are present in trace amounts in the body and play an important role in myriad biological processes including gene expression, signal transduction and metabolic reactions. Abnormalities in the behaviour of these elements often reflect abnormalities in associated bio-molecules and studying them together can offer great insight into many biological
Dr. Shuichi Enomoto, Dr. Shinji Motomura and colleagues, from the RIKEN Center for Life Science Technologies have developed a gamma-ray imaging camera enabling them to detect the gamma-rays emitted by multiple bio-metal elements in the body and study their behavior.

Their second prototype of the system, called GREI–II and presented today in the Journal of Analytical Atomic Spectrometry, enables them to visualize multiple bio-metal elements more than 10 times faster than before, and to do so simultaneously with positron emission tomography (PET).
In the study, the researchers were able to visualise two radioactive agents injected in a tumor-bearing mouse, as well as an anti-tumor antibody labelled with a PET

A chain reaction of toxic proteins may help explain Alzheimer's, Parkinson's and other killers—an insight that could lead to desperately needed new treatment options
Under a microscope, a pathologist searching through the damaged nerve cells in a brain tissue sample from a patient who has died of Alzheimer's disease can make out strange clumps of material. They consist of proteins that clearly do not belong there. Where did they come from, and why are there so many of them? And most important, what do they have to do with this devastating and incurable disorder? The search for answers has turned up a startling discovery: the clumped proteins in Alzheimer's and other major neurodegenerative diseases behave very much like prions, the toxic proteins that destroy the brain in mad cow disease
Prions are misshapen yet durable versions of proteins normally present in nerve cells that cause like proteins to misfold and clump together, starting a chain reaction that eventually consumes entire brain regions. In the past 10 years scientists have learned that such a process may be at work not only in mad cow and other exotic diseases but also in major neurodegenerative disorders, including Alzheimer's, Parkinson's, amyotrophic lateral sclerosis (also known as ALS or Lou Gehrig's disease) and the concussion-related dementia of football players and boxers.

The secret to living longer may be all in your head after all.
A team of neuroscientists has found a way to extend the lives of lab mice by simply switching a brain pathway on and off, according to a paper published May 1 in the journal Nature.
"If we just activated this pathway in the hypothalamus, it accelerated aging," study researcher Dongsheng Cai, of the Albert Einstein College of Medicine, told Business Insider. "If we inhibit this pathway, we can slow down aging. There were lots of assessments that showed inhibiting it led to an increase of lifespan by roughly 20%. So, that's pretty remarkable."
Aging and the brain
The scientists focused on the hypothalamus because it is the region in the brain responsible for growth and metabolism — two things that change as we age. Cai and colleagues have published previous papers on the role of the hypothalamus in age-related metabolic diseases like diabetes, hypertension, and obesity.
But Cai felt that the information on what actually causes aging was lacking. Aging has systemic effects on the body: hitting many different organs and causing many different diseases at once.
He thought that chemicals in the brain associated with age-related diseases, like metabolic syndromes and cancer, might also play a role in aging.
"Aging by itself is not a disease," Cai said, "but it is a risk factor for many diseases. It is more like a ground for the development of many epidemic diseases like diabetes and neurodegenerative disorders."
Stress and inflammation
In mice, the researchers experimented with a protein complex involved in inflammation in the hypothalamus called NF-kB. Inflammation is an overreaction of our body's immune system in response to stress. Inflammation can help heal and fight disease, but too much inflammation can be dangerous.
They were surprised by how much of an impact turning off NF-kB in the hypothalamus had on how long the mice lived — about 20% longer. On the flip side, turning it to overdrive accel

Rudy's new study.

Mass. General study finds protective gene variant promotes clearance of toxic amyloid beta protein from the brain

Massachusetts General Hospital (MGH) investigators have determined that one of the recently identified genes contributing to the risk of late-onset Alzheimer's disease regulates the clearance of the toxic amyloid beta (A-beta) protein that accumulates in the brains of patients with the disease. In their report receiving advance online publication in Neuron, the researchers describe a protective variant of the CD33 gene that promotes clearance of A-beta from the brain. They also show that reducing expression of CD33 in immune cells called microglia enhances their ability to clear away A-beta protein, raising the possibility that blocking CD33 activity could help the brain's immune system remove A-beta.

"Our findings show, for the first time, a "switch" that controls how fast microglial cells can clear A-beta protein from the brain as we age – CD33 is the key," says Rudolph Tanzi, PhD, director of the Genetics and Aging Unit in the MGH Department of Neurology and senior author of the Neuron paper. "If we can find a way of safely inactivating CD33 on microglia, we should be able to slow the accumulation of A-beta in aging brains and hopefully reduce risk for Alzheimer's disease."

In 2008, as part of the Alzheimer's Genome Project, Tanzi's team identified four novel genes containing variants that increased the risk of late-onset Alzheimer's, the most common form of the devastating neurological disorder. One of these was CD33. The protein was known to play a role in regulation of the innate immune system – the body's first line of defense against infection – but how it might function in the brain and possibly contribute to Alzheimer's risk was not known.

In the current study, the researchers first found that CD33 activity was significantly higher in microglia cells in brain samples from Alzh

Amyloid β deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer's disease: a prospective cohort stud

Researchers at the University of Bristol have revealed new insight into the function of a key protein attributed to impaired learning and memory in Down’s syndrome. The findings, published online in Nature Cell Biology, offer further molecular insight into how the reduced level of this key protein termed ‘sorting nexin-27’ [SNX27] may contribute to learning and memory problems associated with Down’s syndrome.

The Bristol-based team now reveal how SNX27 forms the core component of an ancient protein complex which functions to control the abundance of a select group of proteins at the surface of cells. Included among these proteins are numerous transporters that regulate the cell’s ability to take up various nutrients, including glucose and metal ions such as zinc and copper. In cells lacking SNX27, the level of these transporters is reduced and the cell’s ability to take up nutrients is adversely perturbed.

Peter Cullen, Professor of Biochemistry from the University’s School of Biochemistry and senior author of the Wellcome Trust-funded study, said: “Besides the previously recognised role of SNX27 in regulating the synaptic activity of neurones, our study suggests that the lack of SNX27 expression observed in Down’s syndrome may also lead to a reduced metabolic activity that may adversely affect neuronal development and cognitive function.
“Further analysis of the effect of reduced SNX27 expression on the synaptic and metabolic activity of specific neuronal populations will certainly provide much needed molecular insight into the complex neuropathology of Down’s syndrome as well as other neurological conditions.